AJP - Heart and Circulatory Physiology, Vol 257, Issue 3 812-H817, Copyright © 1989 by American Physiological Society
Brief vagal stimuli and AV conduction in dogs: effects on retrograde exceed antegrade
P. J. Martin
Division of Investigative Medicine, Mt. Sinai Medical Center, Cleveland, Ohio 44106.
We opened the chests of 20 mongrel dogs (16-28 kg) that were anesthetized
with pentobarbital sodium (22 mg/kg), given propranolol (1 mg/kg), and
bipolar catheters placed into the right atrium and ventricle. We crushed
the sinoatrial (SA) node and paced the heart to produce either an antegrade
(A-V) or a retrograde (V-A) conduction (where A is atrial activation and V
is ventricular activation). Both cervical vagosympathetic trunks were
ligated and connected to electrodes that were driven by a
computer-controlled, isolated stimulators. Three brief vagal stimulus
bursts (at the same intensity but at different times in the cardiac cycle)
were given at least 1 min apart, the pacing site was changed, and the
identical three-stimulus bursts were again applied. This procedure was
continued until the phase of the stimulus had scanned the entire cardiac
cycle. Forty-four sets of vagal effect curves were generated. The composite
data indicate that brief vagal stimuli have about twice the effect on the
peak amplitude of the change in retrograde than in antegrade AV nodal
conduction in the dog. Unexpectedly, the duration of the parasympathetic
effect is also considerably greater (approximately 40%) and the decay is
slower (approximately 48%) for retrograde than for antegrade conduction,
even when the vagal effect curves have been normalized to the same
amplitude. This latter result suggests that some factor other than
diffusion and inactivation of ACh determines the duration of the A-V
conduction response to a brief vagal stimulus.
